Remicade (Infliximab) is an antibody that blocks the effects of tumour necrosis factor alpha (TNF-alpha). TNF-alpha is
a substance made by the cells of the body (immune system)that has an important role in promoting inflammation. By blocking
the action of TNF-alpha infliximab reduces the signs and symptoms of inflammation.

Malvern,PA--January 2,2001--The U.S. FDA has approved a drug to inhibit the progression of joint damage in patients with
RA a chronic and debilitating disease that affects 2.1 million Americans,mostly women.

The FDA granted marketing approval to Remicade (infliximab) in combination with methotrexate for inhibiting the progression
of structual damage in patients with moderately to severely active RA who have had an inadequate response to methotrexate,alone.

"For the first time,we now have a drug that can inhibit the progression of joint damage as well as control the pain and
stiffness associated with the disease," said Michael Spiegel MD,ATTRACH trial investigator, Danbury,CT."This is excellent
news for patients. Remicade can have a tremendous impact on patients."

Remicade with MTX was first approved for marketing in October 1999 for the treatment of signs and symptoms of RA in patients
who had an inadequate response to MTX.

In patients with RA,joint damage is evident as narrowing of the joint space between bones and erosion of the bones at
the joint space. Remicade inhibits both of these conditions.

"Joint damage progression in RA has two key components,joint space narrowing and joint erosions. Clinical data demonstrates
that Remicade inhibits not only joint erosions but joint space narrowing as well. This provides considerable benefit to patients
while also improving the pain and stiffness associated with the disease,"said Thomas Schable,PhD,senior director,medical affairs,Centocor
Corporation.

Approval was based on 54-week data from the two-year ATTRACT trial (Anti-TNF Trial in RA with Concomitant Therapy),one
of the largest and longer controlled RA clinical trials involving 428 patients at 34 centers in North America and Europe.

In the double blind,placebo-controlled,randomized clinical study,patients treated with Remicade in combination with MTX
were compared to those patients treated with MTX and placebo. MTX is a standard treatment for many patients with RA.

In the ATTRACK trial progression of joint damage was measured radiographically using the van der Heijde modified Sharp
system,which evaluates changes in joint-space narrowing and bone erosion on a 5-point scale(a higher score indicates more
damage).

Among all Remicade treatment groups,overall median change from baseline for radiographic scores of 0.0 were reported
among patients treated with the combination of Remicade plus MTX (n=285) compared to a median change of 4.0 for patients treated
with MTX alone (n=63). A total of 53% of Remicade patients demonstrated 0% progression.

The MTX-only findings (control arm) demonstrated progression compareable to that previously reported for patients with
established RA treated with MTX.

Patients on Remicade plus MTX also reported significantly greater relief from the pain and stiffness of the disease as
well as the reduction in the number of swollen and tender joints.

After 54 weeks of therapy,more than half (52%) of those treated with Remicade and MTX experienced a reduction in the
signs and symptoms of RA as measured by ACR 20,a standard assessment for disease activity,compared to 17% of patients
receiving MTX alone.

In the clinical trials,Remicade was generally well tolerated. The most common adverse events included upper respiratory
infection,headache,mild reactions to the infusion,sinusitis,rash,and cough. There was no increased incidence of serious adverse
events or serious infections in patients receiving Remicade and MTX compared to those receiving placebo and MTX.

The incidence of infusion reactions was low in Remicade plus MTX patients (approx, 3%) for any given infusion compared
to those receiving MTX alone (approx. 2%).

TNF-alpha mediates inflammation and cellular immune respose including response to infection. Serious infections,including
sepis and disseminated tuberculosis,have been reported in patients receiving TNF-blocking agents,including Remicade. Some
of these infections have been fatal.

Many of the serious infections in patients treated with Remicade have occurred in patients on concomitant immunosuppressive
therapy that,in addition to their Crohn's disease or RA,could predispose them to infections.

Caution should be exercised when considering the use of Remicade in patients with chronic infection or a history of recurrent
infection. Remicade should not be given to patients with a clinically important,active infection. Patients should be monitored
for signs and symptoms of infection while on or after treatment with Remicade.New infections should be closely monitored.

If a patient develops a serious infection including sepsis. Remicade therapy should be discontinued. Patients should
be evaluated for the risk of tuberculosis,including latent tuberculosis. Treatment for tuberculosis should be initiated prior
to the treatment with Remicade.

Remicade and other agents that inhibit TNF have been associated in rare cases with exacerbation of clinical symptoms
and/or radiographic evidence of de-myelinating disease. Prescribers should exercise caution in considering the use of Remicade
in patients with pre-existing or recent onset of central nervous system de-myelinating disorders.

Remicade's designers used a very different strategy to make a antibody that could grab onto TNF-alpha and inactivate
it. After the researchers injected mice with human TNF-alpha,the mice made antibodies toward it. Removing just the portion
of the antibody molecule that physically binds to the TNF-alpha,they fused it to a piece of a human antibody molecule.

This meant that they had created antibody molecules that were mouse-human hybrids. Their reasoning was that the mouse
portion would bind to TNF-alpha,while leaving about 75 % of the hybrid from a human source would reduce the chances of the
human recipient with RA recognizing the mouse portion and reject the mouse-human molecules.

The kinds of antibodies that the mouse make against human TNF-alpha are called monoclonal antibodies (mabs). the nobel
Prize-winning techinique of getting mice to make specific antibodies against injected molecules goes back to 1975. Since that
time the use of such antibodies has spread to almost every branch of biomedical research,mainly for detection and diagnosis.

However, by the mid 1990s refinement in the techniques led to a major expansion in research on the use of Mabs for therapy.
By 2000,Mabs were under development for possible therapy against a dozen diseases,including aids/hiv.,diabetes,and especially
cancer. With Remicade,RA joined the ranks of the human diseases targeted by these precisely aimed antibody targetters.

Remicade was initially cleared for marketing in the US in 1998,for short term use in patients with Crohn's disease,a
serious gastrointestinal disorder. Centocor currently markets Remicade in the US. Schering-plough Corporation has rights
to Remicade in all other countries throughout the world except in Japan and parts of the Far East where Remicade will
be marketed by Tanabe Seiyaku Ltd.

Remicade is made from a specially developed antibody (using partial mouse content-referred to as "monoclonal
antibody")originally known as cA2 which acts against TNF.

The use of biologic response modifiers has been under considerable debate in recent months. Many Canadians with RA enjoyed
the benifits of these agents through clinical trials or special access programs,which were in place during the pre-approval
period.

Now that the drugs are approved in Canada,special access programs have ended and most patients cannot afford them. While
most private health plans cover these medications,the majority of provincial plans do not. Provincial formularies cover the
cost of medications for people over the age of 65 or those in need of financial assistance (not true in many cases).

Rheumatoligists across the country are speaking out on behalf of their patients and calling their MPs,MPPs,MLAs,ministers
of health and their deputies to discuss the situation (many falling on deft-ears,except two provincial health care departments).
"We've seen our patients benifit from these medications and they will decline without treatment,"said Dr. Dianne Mosher,a
Halifax rheumatoligist.

"Why do cancer patients,HIV/AIDS patients and others with chronic diseases receive provincial coverage for their medications
and not Canadians with arthritis?" she continued. Remicade is covered by provincial formularies for Crohn's disease,yet it
is refused for RA patients. It's discrimination against our patients pure and simple." (or ignorance of the facts)

To date, only three provinces have listed the drugs,Saskatchewan,British Columbia and Ontario through a special restricted
access program (too discriminatory and restricted in Ontario,it is not clear who is eligable).

Quebec recently denied both medications from its formulary list.

"We are urging the provinces to follow these guidlines (CRA),respect the advice of rheumatologists,the true experts in
arthritis care,and give these patients they need and deserve,"says Denis Morrice,president of the Arthritis Society. "It is
crucial,long-term investments in our health care system,but more importantly,in patients' lives".